(ORDO NEWS) — Our bodies are quite inventive in matters of self-healing, and scientists are studying in detail the ways in which the heart recovers after a heart attack (myocardial infarction). They hope to find clues that could lead to better treatments for cardiovascular problems.
A new study has shown that the body’s immune response and the lymphatic system (part of the immune system) play a critical role in how the heart repairs itself after a heart attack that has caused damage to the heart muscle.
Key to the study was the discovery of the role of macrophages, specialized cells that can destroy bacteria or initiate beneficial inflammatory responses. These macrophages, which are the first to arrive at the scene after a heart attack, produce a special type of protein called VEGFC, the researchers report.
We found that macrophages, or immune cells that rush to the heart after a heart attack to “eat” damaged or dead tissue, also trigger vascular endothelial growth factor C (VEGFC), which triggers the formation of new lymphatic vessels and promotes healing.” says pathologist Edward Thorpe of Northwestern University in Illinois.
The researchers describe this as a Jekyll and Hyde scenario: “good” macrophages producing VEGFC, and “bad” macrophages not producing VEGFC but triggering a pro-inflammatory response that could further harm the heart and surrounding tissues.
In order for the heart to fully recover, dying cells must be removed, a process known as efferocytosis, in which macrophages play an important role. By studying this process in cells in the lab and in mice, the team determined how the right type of VEGFC-producing macrophages do the proper repair job.
Future research may focus on how to increase the number of beneficial macrophages in the heart and reduce or even eliminate damaging macrophages, which will increase the chances of a healthy recovery.
“Our challenge now is to find a way to either inject VEGFC or get these macrophages to induce more VEGFC to speed up the heart’s repair process,” says Thorp.
When people have a heart attack, they are at high risk of heart failure, when the heart becomes unable to continue pumping blood around the body. This risk can be reduced with modern drugs such as beta-blockers, but it still exists.”
While scientists continue to improve our understanding of how heart disease occurs and how we can better diagnose the risk of heart problems early, heart failure continues to kill hundreds of thousands of people a year in the US alone.
Further research like this will shed more light on the biological processes that occur in response to a heart attack – in particular, how the process of efferocytosis is used to trigger the VEGFC protein needed to repair heart muscle.
“We’re looking to better understand how heart failure develops after a heart attack so we can intervene early and change the course of heart recovery,” says vascular biologist Guillermo Oliver of Northwestern University.
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